Risk Of ESKD Research Articles

Circulating proteins linked to apoptosis processes and fast development of end-stage kidney disease in diabetes.

Many circulating proteins are associated with risk of ESKD, but their source and the biological pathways/disease processes they represent are unclear. Using OLINK proteomics platform, concentrations of 455 proteins were measured in plasma specimens obtained at baseline from 399 individuals with diabetes. Elevated concentrations of 46 circulating proteins were associated (P < 1 × 10-5) with development of ESKD (n = 143) during 7-15 years of follow-up. Twenty of these proteins enriched apoptosis/TNF receptor signaling pathways. A subset of 20 proteins (5-7 proteins), summarized as an apoptosis score, together with clinical variables accurately predicted risk of ESKD. Expression of genes encoding the 46 proteins in peripheral WBCs showed no difference between cells from individuals who did or did not develop ESKD. In contrast, plasma concentration of many of the 46 proteins differed by this outcome. In single-nucleus RNA-Seq analysis of kidney biopsies, the majority of genes encoding for the 20 apoptosis/TNF receptor proteins were overexpressed in injured versus healthy proximal tubule cells. Expression of these 20 genes also correlated with the overall index of apoptosis in these cells. Elevated levels of circulating proteins flagging apoptotic processes/TNF receptor signaling pathways - and likely originating from kidney cells, including injured/apoptotic proximal tubular cells - preceded the development of ESKD.

Primary FSGS Patient Response to Immunosuppression (IS) and Risk of ESKD

Primary FSGS Patient Response to Immunosuppression (IS) and Risk of ESKD

Risk of ESKD in ANCA-Associated Glomerulonephritis at Presentation and during the Disease Course

Risk of ESKD in ANCA-Associated Glomerulonephritis at Presentation and during the Disease Course

Heart Failure with Preserved Ejection Fraction (HFpEF), Heart Failure with Reduced Ejection Fraction (HFrEF), and the Risk of ESKD in Type 2 Diabetes (T2D)

Heart Failure with Preserved Ejection Fraction (HFpEF), Heart Failure with Reduced Ejection Fraction (HFrEF), and the Risk of ESKD in Type 2 Diabetes (T2D)

End-stage and chronic kidney disease in classic bladder exstrophy: A retrospective muti-institutional cohort study

IntroductionWhile most children with classic bladder exstrophy (CBE) are born with normal kidneys, some experience renal deterioration in adulthood. Little is known about the incidence of end-stage and chronic kidney disease (ESKD and CKD, respectively) in this population. Our group has recently published on surgical outcomes in a multi-institutional cohort of 216 people with CBE. Our aim was to describe the incidence of ESKD and prevalence of CKD in this cohort of people with CBE. MethodsWe retrospectively reviewed records of patients with CBE followed at five tertiary care centers described previously. The primary outcome was incidence of ESKD, defined as permanent peritoneal/hemodialysis or renal transplantation. The secondary outcome was prevalence of CKD stage 3 or higher (CKD3+, estimated glomerular filtration rate [eGFR]<60ml/min/1.73m2) at the last appointment. Creatinine-based eGFRs were calculated using the CKD-EPI Creatinine Equation (adults) and the Schwartz formula (children). Survival analysis and Fisher’s exact test were used. ResultsA total of 201 patients (93% of the original cohort) had renal function data available (63% male). Four patients who had a primary urinary diversion remained diverted at a median follow-up of 20.1 years. None developed ESKD and one developed CKD3+. The remaining 197 patients had a primary bladder closure. At a median follow-up of 18.8 years old, 12 were diverted, 108 were augmented and 77 were neither. Three patients developed ESKD (1.5%) at a median age of 23.4 years (1 hemodialysis, 2 transplantation). On survival analysis, the risk of ESKD was 0% at 10 years, 1% at 20 years and 5% at 30 years (Figure). This was higher than the risk of 0.003% at 21 years of age in the general population (p<0.001). The median age of 141 individuals with eGFR data was 21.6 years old (65% male). No children, 4% of adolescents and 8% of adults had CKD3+ (p=0.45). On exploratory analyses, prevalence of CKD3+ did not differ by center or birth year (p>=0.99). ConclusionsThe risk of ESKD and CKD among patients with CBE is not insignificant and appears to be more common than the general population. The potential role of modifiable contributing factors, such as increased bladder outlet resistance, warrants further investigation. Reliable long-term follow up is needed in this population to monitor for ESKD and CKD.

Intensive Home Blood Pressure Lowering in Patients with Advanced CKD

Optimal blood pressure (BP) targets in advanced CKD are controversial. More intensive BP lowering in the setting of advanced CKD is thought to be associated with risk of acute kidney injury, hyperkalemia, and ESKD. We aimed to conduct a pilot trial of intensive BP control to determine if lower SBP targets can be safely achieved for patients with CKD through titration of BP medications using in-home measured BP. Non-blinded randomized controlled trial. 108 patients with advanced CKD (eGFR ≤30 mL/min/1.73 m2) and hypertension. Participants were randomized either to a target home SBP goal of <120 mmHg (N=66) or a less intensive SBP goal (N=42). Antihypertensive medications were titrated to achieve the target home SBP range in the first 4 months of the study and maintained until the end of the study. Home BP was measured using a wireless Bluetooth-enabled monitor that transmitted readings to providers in real-time. The primary efficacy outcome was the difference in achieved clinic SBP between the two study arms from months 4-12. Safety outcomes included hyperkalemia, a composite outcome of falls or syncope, and onset of need for dialysis or kidney transplantation. The mean clinic SBP at month 12 was 124.7 mmHg in the intensive SBP group vs. 138.2 mmHg in the less intensive SBP group. Averaged over months 4-12, the achieved mean clinic SBP in the intensive SBP arm was 11.7 mmHg (95% CI 7.5 to 16 mmHg, p<0.001) lower than the mean SBP achieved in the less intensive SBP arm. Primary safety outcomes were not statistically significantly different between the two arms (all p>0.05). Small sample size which may limit our ability to detect clinically significant differences in rates of adverse outcomes; single-center design. A clinic SBP goal of <120 mmHg is feasible to achieve with the help of real-time home BP monitoring and appears to be safe in this study population with advanced CKD. Larger trials to determine optimal BP targets in advanced CKD and the risks and benefits associated with more intensive BP control are warranted.

Dietary Sodium and Potassium Intake and Risk of CKD Progression, ESKD, or Death in the Million Veteran Program

Dietary Sodium and Potassium Intake and Risk of CKD Progression, ESKD, or Death in the Million Veteran Program

Discrepancy between Lifetime Risk of ESKD vs. 3-Year Risk of CKD Progression in US Adults with Diabetes

Discrepancy between Lifetime Risk of ESKD vs. 3-Year Risk of CKD Progression in US Adults with Diabetes

Long-Term Risk of ESKD in Kidney Donors with Diabetes Mellitus Using eGFR 6 Months after Donation

Long-Term Risk of ESKD in Kidney Donors with Diabetes Mellitus Using eGFR 6 Months after Donation

Hyperuricemia Treatment Reduces ESKD Risk and Mortality in Patients with CKD: A Causal Inference Analysis Using the G-formula Approach

Hyperuricemia Treatment Reduces ESKD Risk and Mortality in Patients with CKD: A Causal Inference Analysis Using the G-formula Approach

Estimates of eskd risk and timely kidney replacement therapy education

BackgroundKidney replacement therapy (KRT) needs preparation and its timing is difficult to predict. Nephrologists’ predictions of kidney failure risk tend to be more pessimistic than the Kidney Failure Risk Equation (KFRE) predictions. We aimed to explore how physicians’ risk estimate related to referral to KRT education, vs. the objective calculated KFRE.MethodsProspective observational study of data collected in chronic kidney disease (CKD) clinics of the Veterans Affairs Medical Center San Diego and the University of California, San Diego. The study included 257 participants who were aged 18 years or older, English speaking, prevalent CKD clinic patients, with estimated glomerular filtration rate (eGFR) < 60 mL/min per 1.73 m2 (MDRD equation). The exposure consisted of end stage kidney disease (ESKD) risk predictions. Nephrologists’ kidney failure risk estimations were assessed: “On a scale of 0–100%, without using any estimating equations, give your best estimate of the risk that this patient will need dialysis or a kidney transplant in 2 years.” KFRE was calculated using age, sex, eGFR, serum bicarbonate, albumin, calcium, phosphorus, urine albumin/creatinine ratio. The outcomes were the pattern of referral to KRT education (within 90 days of initial visit) and kidney failure evaluated by chart review. The population was divided into groups either by nephrologists’ predictions or by KFRE. Referral to KRT education was examined by group and sensitivity and specificity were calculated based on whether participants reached kidney failure at 2 years.ResultsA fifth were referred for education by 90 days of enrollment. Low risk patients by both estimates had low referral rates. In those with nephrologists’ predictions ≥ 15% (n = 137), sensitivity was 71% and specificity 76%. In those with KFRE ≥ 15% (n = 55), sensitivity was 85% and specificity 41%.ConclusionsAlthough nephrologists tend to overestimate patients’ kidney failure risk, they do not appear to act on this overestimation, as the rates of KRT education referrals are lower than expected when a nephrologist identifies a patient as high risk.Clinical Trial NumberNot applicable

#1623 Risk factors for end-stage kidney disease and death in ANCA-associated vasculitis with glomerulonephritis

Abstract Background and Aims ANCA-associated vasculitis (AAV) with glomerulonephritis (AAV-GN) still carries poor prognosis despite treatment improvement over the last years. Currently, improving assessment of disease activity and severity and defining risk factors for ESKD pose challenges. In this study we aim to determine and characterize risk factors associated with progression to ESKD or death in patients with AAV-GN. Method We retrospectively analysed all AAV-GN cases of our Center. ESKD was considered as a composite outcome of eGFR&amp;lt;15 or dialysis dependency. Biopsies were classified according to Berden's classification (BC), Brix's renal risk score (RRS), Mayo Clinic Chronicity Score (MCCS) and AAV-GN combined score (AAV-GN-CS). Categorical variables were analysed by non-parametric chi-square or fisher's exact test; and continuous variables by Mann-Whitney U test. Cox regression models were applied for death and Kaplan-Meier estimator. Significance value α = 0.05 was considered. Results A total of 74 patients, 56.8% male, 69 years-old median age were included. Of them, 81.2% were MPO, 11.6% PR3 and 7.2% negative. At presentation, 35.3% had alveolar haemorrhage, 13.4% GI and 66.7% constitutional manifestations. At diagnosis, median eGFR was 7.5 mL/min/1.73 m2 (5.0-13.0), proteinuria 2.2g/g (0.45-4.17) and all patients had haematuria. Initial median ANCA titer (ATi) was 100 UI/mL (51-134) and at last follow-up 44 (15-101). 64.2% of all patients required dialysis at presentation. Of these, 14.0% recovered until discharge. We also analyzed biopsies of 57 patients. According to BC, 15.8% were focal, 40.4% crescentic, 26.3% mixed, and 17.5% focal. ESKD risk was medium in 28.3% and high in 69.8%, as determined by RRS; whereas low in 31%, intermediate in 42.3% and high in 19% as per AAV-GN-CS. Induction treatment (IT) used was cyclophosphamide (CYC) in 46.3%, CYC plus rituximab (RTX) in 18.3% and RTX in 3.3%. Only 17 patients (26.2%) were added plasmapheresis (PLEX). Only 28% achieved kidney remission (KRm), 7% relapsed and 68.7% developed ESKD. Of them, 95.5% had eGFR&amp;lt;15 at diagnosis, 30% low C3, 37.5% crescentic pattern, 28.1% mixed and 28.1% sclerotic. 87% of ESKD patients had &amp;lt;25% normal glomeruli (NG), and 87.1% high ESKD risk (RRS). Progression to ESKD was associated with lower eGFR (p &amp;lt; 0.001) and low C3 at diagnosis (p = 0.026), lower %NG (p = 0.004), higher %CG (p = 0.004), higher %IFTA (p = 0.011), worse BC (p = 0.012), higher RRS (p &amp;lt; 0.001) and MCCS categories (p = 0.010), but not with AAV-GN-CS. ATi reduction seems to determine better renal outcome (p = 0.042). No significant differences were seen with IT or maintenance treatment, nor with PLEX addition. No patient treated with RTX, or combined treatment developed ESKD. Mortality was 32.8% and the best predictive model includes age, GI manifestations and KRm (p &amp;lt; 0.001). Age (p = 0.004), lower eGFR at diagnosis (p = 0.016) and GI manifestations (p = 0.003) were predictive of death, while achieving KRm improved survival (p = 0.009). Conclusion Our results reveal that AAV-GN patients have poor kidney outcome when presenting with severe kidney dysfunction, high ANCA titers and low C3 levels. Worse histological scoring is determinant of ESKD. The prediction power of AAV-GN-CS must be demonstrated in large cohorts. RTX effectivity on kidney survival must be further supported. Patient survival is related with younger age at diagnosis, organ systems involved at clinical presentation, and achievement of kidney remission.

#1716 IgA nephropathy: our center's experience

Abstract Background and Aims IgA Nephropathy (IgAN) is the most common primary glomerulopathy worldwide. In the last years, significant advances have been made in understanding its pathophysiology and developing newer promising treatments. The accuracy of the International Risk-Prediction Tool in IgAN (IRP-IgAN) was already validated. Herein, we retrospectively analysed the relation of this risk score and the kidney outcomes. Method We performed a single center retrospective observational cross-sectional study of patients with histological diagnosis of IgAN between 2015 and 2023 in Centro Hospitalar de Setúbal, aiming to describe the demography, clinical presentation, histological characteristics, treatment and follow up of our cohort. The International Risk-Prediction Tool in IgAN was applied for patient stratification. Results Twenty-eight patients were diagnosed with IgAN in this eight-year period. Mean age was 46 years-old (SD ±12.2) and 71.4% were male. The majority were Caucasian (n = 26) with only two patients of Asian e African descent, respectively. The mean calculated Charlson Comorbidity Index was 1.43 (SD ±1.5). Eighteen patients (64.3%) had known arterial hypertension, diabetes was seen only in 2 patients, obesity in 4 patients, and hepatitis B in 2 patients. No cardiovascular disease or cancer was documented. On presentation, 71.4% (n = 20) had hypertension, 14.3% (n = 4) presented with rapidly progressive renal insufficiency, and 14.3% (n = 4) presented with nephrotic syndrome. Two patients (7.1%) required dialysis on presentation. Also, the mean glomerular filtration rate (GFR) was 55.3 ml/min (SD ±31.9) and mean proteinuria level (protein-to-creatinine ratio) was 2.42g/g (SD ±2.41). Most patients had hematuria (82.1%), C3 consumption was seen in only one patient while 10 patients had isolated higher levels of IgA. Mean time between the first symptoms or documented clinical features and dedicated Nephrology consultation was 2.9 years (SD ±3.78). Regarding the histological data and considering de MEST-C score, 71.4% had mesangial hypercellularity in more than 50% of the glomerulus (M1), 25% had endocapillary hypercellularity (E1), 17% had segmental glomerulosclerosis of at least one glomerulus (S1), 7% had interstitial fibrosis or cortical atrophy in 25-50% of the cortical area (T1) and 11% in more than 50% (T2), 17.9% had crescents in less than 25% of the glomerulus (C1) and 2.6% in more than 25% (C2). Fibrinoid necrosis was noticed in 7.1% of the patients. The presence of IgA in the mesangium on IF was universal and 18 patients (64.3%) had C3 co-stain. Approximately half of the patients (46.4%) were already on angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blockers (ARB) by the time of clinical presentation and nearly all (92.9%) by the time the diagnosis was established. SGTL-2 inhibitors were started in 42.9% of the patients. Eight patients (28.6%) started immunosuppression therapy, within a mean time from histological diagnosis of 0.7 years (SD ±1.03). Of those, all of them were on corticosteroids, one patient was additionally under oral cyclophosphamide and another one under mofetil mycophenolate. According to the IRP-IgAN, patients were stratified in low (35.7%), intermediate (10%) and high risk (8%) of kidney disease progression (GFR decline &amp;gt;50%) or ESKD. In a mean time of 0.53 (SD ±0.34) years of follow-up after diagnosis, 8 patients (28.6%) required renal replacement therapy, with 7 choosing hemodialysis and 1 peritoneal dialysis. Six patients lost follow-up. Three patients died a mean time of 1.2 years after diagnosis, one from immunosuppression-related adverse events. We also found an association between higher risk group and progression to ESKD (p &amp;lt; 0.001). Conclusion The IRP-IgAN tool is a useful tool for prediction of kidney disease progression and the need for renal replacement therapy. The supportive care in IgAN even with antiproteinuric approach could be insufficient for patients with high and intermediate risk. The risk progression to ESKD is indeed heterogeneous, and close follow-up of these patients should be guaranteed.

#1283 Rituximab in addition to plasma exchange, cyclophosphamide and steroids for treatment of anti-GBM disease

Abstract Background and Aims Anti-GBM disease is a rare antibody-mediated vasculitis, usually treated with plasma exchange (PEX), cyclophosphamide (CYC) and steroids. There are limited data regarding the use of B-cell depleting therapies such as rituximab (RTX). We investigate the use of the addition of rituximab for the treatment of Anti-GBM disease. Method Ten-year (2012-2023) single-centre retrospective cohort study of patients with anti-GBM disease treated with or without rituximab, in addition to standard care, as first-line therapy. A Cox-proportional hazards regression model incorporating age, sex, ANCA status, dialysis need at presentation, lung haemorrhage, CYC (oral or IV) and RTX treatment was used to identify disease/treatment factors associated with outcome (death, end-stage kidney disease [ESKD], infection). Results Forty-five patients are included; baseline demographics, disease characteristics, treatments and outcomes are summarised in Table 1. In the Cox regression model, only increasing age was associated with risk of death (HR 1.08 [95% CI 1.02-1.17]). Age (HR 1.04 [1.01-1.08]), female sex (HR 4.93 [1.80-4.87]), and dialysis need at presentation (HR 5.28 [1.54-17.53]) were associated with ESKD-risk. Increasing age (HR 1.04 [1.00-1.09] and ANCA positivity (HR 3.08 [1.14-8.71]) were associated with risk of infection. The addition of rituximab was not significantly associated with risk of death (HR 0.82 (0.24-2.87), ESKD (HR 1.54 [0.64-3.96]) or infection 2.06 [0.67-5.71]. Conclusion Addition of rituximab to standard treatment for anti-GBM disease was not associated with improved renal outcome or survival benefit. However, rituximab use permitted lower cumulative doses of CYC and reduction in the number of PEX, without an increased risk of infection. Rituximab may have a role as a CYC- and PEX-sparing treatment in patients with anti-GBM disease.

#2213 APOL1 high-risk genotype in in a Dutch multi-ethnic population

Abstract Background and Aims The presence of 2 APOL1 high-risk alleles (high-risk APOL1 genotype) is associated with an increased risk of ESKD. In the USA, the prevalence of these high-risk alleles is high in people of West African descent and almost absent in patients from European descent. In Amsterdam, there is a significant number of people from Surinam, and (West-) Africa. A big group of Surinamese individuals have a West African heritage. The prevalence, however, of high-risk APOL1 genotype in the Netherlands and thereby the significance is unknown. The aim of this research was to investigate the prevalence of the APOL1 risk alleles in a multi-ethnic cohort of the Amsterdam general population consisting of individuals of African Surinamese, Ghanaian, Moroccan and Dutch origin. Second we correlate the presence of these risk alleles to blood pressure, kidney function and proteinuria. Method HELIUS is a multi-ethnic prospective cohort study including people aged 18-70 who were randomly selected, stratified by ethnic origin, from the Amsterdam general population. Baseline examination took place tween 2011 and 2015. We analysed a population of 5971 individuals with available genotype data, of whom 1287 were of Dutch, 3048 of Moroccan, 1156 of African Suriname and 480 of Ghanaian descent. APOL1 risk was determined by genotyping two APOL1 missense variants, rs73885319A&amp;gt;G, S342G; rs60910145T&amp;gt;G, I384M, together constitute the G1 high-risk allele and the 6-base pair deletion allele, rs71785313 RRRATAA/−, N388Y399/−−, is the G2 high risk allele. Logistic regression analyses were performed to determine correlation between creatinine, eGFR, and systolic blood pressure and apol1 high risk genotype, with additional adjustments for age, sex, and BMI. Results The prevalence of high-risk APOL1 genotype was 4.17% in the total sample, in African Surinamese 9.5%, and in the Ghanaian 29.0%. There were no individuals with high risk genotype in the Moroccan or Dutch descent population. The presence of high risk APOL1 genotype was associated with an elevated creatinine level of 10.68 µmol/L (SD 0.91) in the whole cohort. Also, in the Surinamese and Ghanaian populations population the presence of the high-risk APOL1 genotype was associated with an increased creatinine of 2.6 µmol/L (SD 1.00) as compared to the black population with low-risk APOL1 genotype. People with high-risk APOL1 genotype had significantly higher systolic blood pressure 10.69 mmHg (SD 0.091) than those without. Nevertheless, there was no significant difference in systolic blood pressure in the black population with high-risk APOL1 genotype in comparison with the black population with low-risk APOL1 genotype 1.38 mmHg (SD 1.17). Also, there was no significant difference in eGFR (CKD CKD-EPI 2009) in any analysis and no differences in proteinuria was seen, between those with and without the high-risk APOL1 genotype. Conclusion In this population, the overall prevalence of the APOL1 risk alleles seems to conform to the African American population in the USA. There is however a much higher prevalence of high-risk APOL1 genotype in the Ghanaian in comparison to the African Surinamese. The group with high-risk APOL1 genotype had significantly higher creatinine levels and higher systolic blood pressure. However there was no significant difference in blood pressure within the black population between APOL1 high-risk genotype and low-risk genotype. There was no significant difference in eGFR, possibly because the CKD-EPI 2009 formula was used which overestimates the eGFR in the black population. Better calculation with cysteine C possibly gives different outcomes. In conclusion, this is the first study in Europe investigating the prevalence of APOL1 high-risk genotype in a large population-based cohort. APOL1 risk alleles, and high-risk genotype, are prevalent in our population of African descent. More analysis in this cohort are pending and also longitudinal data will follow.

Suitability of reduced dose glucocorticoids therapy regimen for antibody-associated vasculitis patients with TB: a retrospective study.

Immunosuppressive therapy is the major treatment approach for patients with anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV). Due to impaired cellular immunological function and the use of glucocorticoids and immunosuppressants, AAV patients are predisposed to opportunistic infections, including tuberculosis (TB). This retrospective study aims to analyze the clinical characteristics of patients with AAV and TB and explore suitable glucocorticoid regimens for them. So as to provide a basis for future clinical guidelines and have important value for guiding clinical treatment. This study retrospectively reviewed 58 AAV patients (18-80 years old) with TB admitted to Changsha Central Hospital Affiliated with the University of South China from 2016.1 to 2023.4 Patients were divided into standard-dose and reduced-dose glucocorticoid groups before retrospectively analyzing their medical records. A total of 58 AAV patients with TB were enrolled, with 15 dying throughout the monitoring period. Through analysis data, compared with the standard-dose group, the reduced group had less proteinuria and hematuria. In survival analysis, the reduced-dose glucocorticoid group had lower mortality than the standard-dose group (P = 0.03); however, no significant difference was noted in the use of immunoglobulin (P = 0.39), tuberculosis activity (P = 0.64), and age stratification (P = 0.40). The BVAS score before treatment and 6 months post-treatment suggest that the two regimens cause the same risk of ESKD (P > 0.05). In conclusion, the reduced glucocorticoid dose group can achieve the same curative effect as the standard dose group and has less damage to the kidney in hematuria and proteinuria. Therefore, the reduced glucocorticoid dose treatment regimen may be more suitable for AAV patients with TB.

Health Inequity in Likelihood and Time to Renal Recovery after Living Kidney Donation: Implications for Kidney Health in Black Americans.

Live donor kidney transplantation has been popularized to help mitigate the organ shortage crisis. At the time of living donor nephrectomy, living donors lose 50% of their kidney function or glomerular filtration rate (GFR). Studies have shown that in healthy living donors, the remaining kidney is able to adapt and recover 10% to 25% of postdonation lost GFR. GFR recovery is critical to long-term kidney health, particularly for Black Americans who disproportionately suffer from kidney disease with an incidence 2.5 times White Americans. To date, no study has examined whether health inequities in renal recovery postdonation exist. We retrospectively analyzed 100,121 living kidney donors reported to the Scientific Registry of Transplant Recipients between 1999 and 2021. We estimated GFR (eGFR) using the Chronic Kidney Disease Epidemiology Collaboration 2021 equation and predicted the likelihood (logistic regression) and time (Cox regression) to recovery of 60% and 75% predonation eGFR. Models adjusted for age, sex, race, BMI, and predonation eGFR. Black patients were 47% (adjusted odds ratio 0.53, 95% CI 0.50 to 0.56, p < 0.001) and 43% (adjusted odds ratio 0.57, 95% CI 0.54 to 0.60, p < 0.001) less likely to recover 60% and 75% of predonation eGFR, respectively, compared with their White counterparts. The hazard ratio for time to renal recovery of 60% and 75% of predonation eGFR was 22% (adjusted hazard ratio 0.78, 95% CI 0.76 to 0.80, p < 0.001) and 38% (adjusted hazard ratio 0.62, 95% CI 0.60 to 0.65, p < 0.001) lower, respectively, than White patients. Black living kidney donors were less likely to recover predonation eGFR, and time to renal recovery was significantly longer than their White counterparts. These data highlight the need for enhanced living kidney donor follow-up, particularly for Black living kidney donors who are at greatest future risk of end-stage kidney disease.

Successful glucocorticoid withdrawal in Chinese lupus nephritis patients: A single centre experience

ObjectiveTo evaluate the proportion of patients successfully withdrawn from glucocorticoids (GC) in a longitudinal cohort of patients with lupus nephritis over a period of 20 years, clinical and pathological predictors of patients with GC withdrawal and renal outcomes after GC withdrawal were further explored. MethodsPatients with successful GC withdrawal were identified for the cohort, and the following data were collected: demographic characteristics, clinical manifestations, pathological findings at disease onset, flares, and renal outcomes subsequent to GC withdrawal. ResultsThere were 365 patients with lupus nephritis included with a median follow-up of 109.5 (83.5,165.3) months in our cohort. A total of 21 patients (5.8 %) achieved successful GC discontinuation, with a median duration of 7.5 (3,10) years necessary for GC withdrawal. The average duration of GC reduction from 7.5 mg/d to complete withdrawal lasted for approximately 25 months (18,30). Patients in the GC-withdrawal group had a lower prevalence of nephrotic syndrome (NS) at onset (28.5 % vs. 47.3 %, P = 0.035), a higher prevalence of positive anti–double-stranded DNA (anti-dsDNA) antibody (85.7 % vs. 61.6 %, P = 0.028) and more severe endocapillary hypercellularity in the renal histopathology evaluations (3(2.5,3) vs. 3(2,3), P = 0.022). NS at disease onset was an independent risk factor to predict unachievable GC withdrawal (OR 0.296, 95 % CI (0.104,0.842), P = 0.022) by multivariate analysis. With a median follow-up of 34 (20,42) months, none of these patients had flares after GC withdrawal. ConclusionsThe discontinuation of GC therapy in LN patients with complete remission and a stable treatment regimen for at least 5 years was feasible without an increased risk of flares, ESKD or death. Low-dose GC withdrawal necessitates a prolonged duration of time and meticulous monitoring.

Risk of ESKD and Death Among Homeless Veterans with Incident CKD

Risk of ESKD and Death Among Homeless Veterans with Incident CKD

CKD stage-specific utility of two equations for predicting 1-year risk of ESKD.

The Kidney Failure Risk Equation (KFRE) and Kaiser Permanente Northwest (KPNW) models have been proposed to predict progression to ESKD among adults with CKD within 2 and 5 years. We evaluated the utility of these equations to predict the 1-year risk of ESKD in a contemporary, ethnically diverse CKD population. We conducted a retrospective cohort study of adult members of Kaiser Permanente Northern California (KPNC) with CKD Stages 3-5 from January 2008-September 2015. We ascertained the onset of ESKD through September 2016, and calculated stage-specific estimates of model discrimination and calibration for the KFRE and KPNW equations. We identified 108,091 eligible adults with CKD (98,757 CKD Stage 3; 8,384 CKD Stage 4; and 950 CKD Stage 5 not yet receiving kidney replacement therapy), with mean age of 75 years, 55% women, and 37% being non-white. The overall 1-year risk of ESKD was 0.8% (95%CI: 0.8-0.9%). The KFRE displayed only moderate discrimination for CKD 3 and 5 (c = 0.76) but excellent discrimination for CKD 4 (c = 0.86), with good calibration for CKD 3-4 patients but suboptimal calibration for CKD 5. Calibration by CKD stage was similar to KFRE for the KPNW equation but displayed worse calibration across CKD stages for 1-year ESKD prediction. In a large, ethnically diverse, community-based CKD 3-5 population, both the KFRE and KPNW equation were suboptimal in accurately predicting the 1-year risk of ESKD within CKD stage 3 and 5, but more accurate for stage 4. Our findings suggest these equations can be used in1-year prediction for CKD 4 patients, but also highlight the need for more personalized, stage-specific equations that predicted various short- and long-term adverse outcomes to better inform overall decision-making.